In a message dated 7/6/00 6:06:37 AM, joao.magalhaes@fundp.ac.be writes:
>>The problem for "aging gene" theory is not so much the wide effects
>>of aging as the variability.
>
>What variability? I said before that there are great similarities in the
>aging process of all well-studied mammals.
They have the same types, but widely differing quantities. An aging
pathology which is the primary limitation for one individual or strain
is irrelevant for another of the same species.
>I've got another question, why don't reptilians or amphibians show
>widespread aging?
They do show widespread aging. The only sexual species for which I've
ever seen a "non-aging" claim are extremely long-lived ones like
lobsters. Even with those species, there's a problem with catch
records. If they didn't age, we should find some 200-year old
lobsters; but we don't.
>Even species such as Desmognathus that live less than 15
>years do not show signs of increased mortality with age (in fact, they
>show decreased mortality after adulthood is reached).
Do you have a cite for this?
>I'm not saying helicases cause aging. I'm just saying that they control many
>age-related pathologies, disproving your theory that age-related pathologies
>are caused by independant genes.
They don't control any aging phenotype; most individuals in a species
have the same helicases; but they will vary greatly in the frequency
of any particular aging phenotype.
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